Early life stress (ELS), including abuse, neglect, and loss, is associated with dramatic increases in lifelong risk for the development of mental and physical health difficulties. The mechanisms through which ELS confers risk for these negative outcomes, however, are not well understood. Stressful life experiences activate the stress response systems, and high levels of stress have been linked to telomere shortening, an epigenetic marker of aging. Thus, shorter telomere length may be one mechanism through which ELS leads to negative health outcomes later in life. In the proposed study we will examine the association of ELS with a measure of cellular aging, as well as with measures of mental and physical health during childhood. More specifically, we will examine in a large sample of pre-pubertal boys and girls the association between ELS and telomere length, as well as rate of telomere attrition across the pubertal period as a function of early experiences of stress. We will also examine the link between ELS and irritability, a common characteristic of several psychiatric disorders, that has been associated with more severe and chronic forms of mental health difficulties. In addition, we also will examine the association between ELS and physical health, given that global measures of health in childhood are likely to precede the onset of specific diseases of aging in adulthood. Finally, we will examine the degree to which variability in telomere length explains increased irritability and physical health problems in individuals with a history of ELS, in order to test a potential mechanism by which early adverse experiences result in maladaptive outcomes. The results of this study will not only increase our understanding of the relations among ELS, telomere length, and health outcomes, but will also provide insight into a markers of cellular aging longitudinally during the important developmental period of adolescence, a stage of increased risk for the onset of mental health difficulties following ELS. Thus, we anticipate that the current study will contribute to our understanding both of models of the onset of psychopathology following ELS and of mechanisms by which ELS confers heightened risk for negative health outcomes. Findings from the proposed study will increase our knowledge of biological responses to stress and will provide insight into the onset and progression of disease following early adversity.